A new study brings us one step closer to “the ‘holy grail’ of heart research:” heart regeneration. When injected in rodents, a new protein triggers a process that helps the heart to recover following an attack.
Almost 800,000 people in the U.S. have a heart attack every year, with 1 in 5 people not even being aware that they had one.
During a heart attack, or a myocardial infarction, the oxygen-carrying blood flow does not reach the heart.
Because of the oxygen deprivation, cells begin to die — thereby damaging a person’s heart muscle.
This causes the immune system to dispatch immune cells to the “injury site” in an attempt to get rid of the dead cells. However, these immune cells also cause inflammation, which leads to cardiac fibrosis.
In the long-term, the damage caused by the immune cells is greater than their help. The scar tissue in cardiac fibrosis does not contract, impairing the heart’s ability to pump blood. Ultimately, this could lead to heart failure.
So far, medical scientists have not managed to find a solution to this problem. But now, a team led by researchers at Oxford University in the United Kingdom may have found a protein that, when injected after a heart attack, reduces heart muscle damage and helps the heart to regain its pumping function.
The new study was led by Paul Riley, a professor of regenerative medicine at the British Heart Foundation (BHF) Centre of Regenerative Medicine at Oxford University.
The results were published in the Journal of Clinical Investigation.
Prof. Riley and colleagues designed a mouse model of a heart attack. Then, they injected a protein called VEGF-C in some of the rodents and left another group untreated.
In the treated group, the researchers were able to see that the protein caused the growth of a network of lymphatic vessels.
They noticed that these lymphatic vessels helped to clear the immune cells after having helped with heart repair and cell debris clearing.
So, the immune cells were at the injury site just long enough to help recovery, but not too long so as to cause more damage.
This treatment-induced process allowed the heart to recover its pumping ability almost entirely. And by comparison, the untreated rodents lost almost half of their heart function.
Prof. Riley explains the mechanism behind the findings, saying, “We now know that it’s not enough to just get healing immune cells into the heart.”
“We need to boost the routes that remove these immune cells once they’ve done their job, so that they don’t start causing more harm,” he adds, “and ultimately contribute to the long-term damage that leads to heart failure.”
“This research has allowed us to start a drug discovery program to develop drugs to promote the growth of lymphatic vessels and quickly clear immune cells. We hope to get a treatment we could give to people after a heart attack within 5–10 years.”
Prof. Paul Riley
Prof. Jeremy Pearson — an associate medical director at the BHF — also chimes in, saying, “Heart regeneration is the ‘holy grail’ of heart research. [The] findings bring us one step closer to understanding how to turn this into a reality.”
“Exploiting the lymphatic system,” continues Prof. Pearson, “opens up new opportunities to find treatments that will limit the damage caused by a heart attack and promote regeneration.”